Purpose: Epidemiological and ecological evidences suggest a positive association of overweight and obesity with the risk of testicular germ cell cancer (GCC). Previous controlled trials reported conflicting results. The present study aimed to analyse the putative association of overweight with GCC risk in a large patient sample and to summarize previous data.
Methods: A total of 8,498 GCC patients were enrolled in a nationwide multicentric case control study. Self-reported body dimensions were recorded for calculation of the body mass index (BMI; kg/m(2)). For comparison, 2,070 age-matched male probands of the latest German National Health Survey (NHS) were employed. Patients and controls were categorized according to age as follows: 18-29, 30-39, and 40-49 years, respectively, and according to BMI, as follows: <18.5; 18.5 to <25; 25 to <30; >30 kg/m(2), respectively. Frequencies of BMI-categories in the three age groups were tabulated and compared statistically. The literature was searched for previous controlled trials regarding BMI and GCC risk.
Results: The median BMI of all GCC patients is 24.69 kg/m(2). Overall comparison of frequencies of BMI categories of cases and controls did not reveal any significant difference. However, in young men (18-29 years) BMI categories 25 to <30 kg/m(2) and >30 kg/m(2) were significantly more frequent in GCC patients than in controls (p < 0.00001). Nineteen previous studies were identified in the literature, one of which being clearly in accordance with the present hypothesis, one being antithetical while the remaining studies were inconclusive in various aspects.
Conclusion: The results of this population-based study lend support to two hypotheses regarding the pathogenesis of GCC: First, as high-calorie nutrition is the most important reason for increased BMI, it appears conceivable that nutritional factors are involved in the pathogenesis of GCC. Second, as nonseminoma is the most prevalent histological subtype among younger patients, the association of increased BMI with incidence of GCC in this particular subgroup may point to divergent pathogenetic pathways of nonseminoma and seminoma, respectively.